Abstract
Two human alpha 2-adrenergic receptor subtypes, alpha 2A-C10 and alpha 2C-C4, were compared with respect to their ability to inhibit stimulated cAMP-production. The inhibition was transduced with about one order of magnitude higher sensitivity in the alpha 2C-C4 subtype than in the alpha 2A-C10 subtype. The phorbol ester, TPA, known to desensitize alpha 2-adrenergic receptor function, possible through phosphorylation of Gi, almost completely abolished the inhibition of cAMP-production in the alpha 2C-C4 subtype, while only a partial effect was seen in the alpha 2A-C10 subtype. These results suggest that the receptor subtypes differ with respect to their coupling efficiency to adenylyl cyclase.
Publication types
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Comparative Study
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Research Support, Non-U.S. Gov't
MeSH terms
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Adenine / metabolism
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Adenylyl Cyclases / metabolism*
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Adrenergic alpha-Antagonists / pharmacology
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Clonidine / pharmacology
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Colforsin / pharmacology
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Cyclic AMP / metabolism*
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Fibroblasts / metabolism
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Humans
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Imidazoles / pharmacology
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Kinetics
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Medetomidine
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Norepinephrine / pharmacology
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Receptors, Adrenergic, alpha-2 / classification
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Receptors, Adrenergic, alpha-2 / drug effects
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Receptors, Adrenergic, alpha-2 / physiology*
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Tetradecanoylphorbol Acetate / pharmacology*
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Transfection
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Yohimbine / metabolism
Substances
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Adrenergic alpha-Antagonists
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Imidazoles
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Receptors, Adrenergic, alpha-2
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Colforsin
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Yohimbine
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Cyclic AMP
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Adenylyl Cyclases
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Adenine
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Clonidine
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Medetomidine
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Tetradecanoylphorbol Acetate
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Norepinephrine